ciated with these rodent-borne hemorrhagic fevers and hantavirus pulmonary syndrome generate great concern in the medical, scientific, and public health communities—and among the general public. Rodent-borne diseases will undoubtedly continue to emerge and increase in medical significance in many areas of the world.
Ecological and environmental conditions determine the epidemic potential of pathogens transmitted by animal reservoirs. Transmisson of arena-viruses—such as Junin virus (found in the corn mouse, Calomys musculinus) in Argentina, Machupo virus (in Calomys calosus) in Bolivia, and Lassa virus (from multimammate rats [Mastomys spp.]) in Africa—has strong environmental determinants. Transmission of each of these pathogens occurs via contact with rodent urine, feces, or tissues; the stability of the pathogens is influenced by humidity and sunlight. A strong link exists between the density of rodent reservoirs and arenaviral diseases in humans. For example, a longitudinal study of C. musculinus populations in an area in which Argentine hemorrhagic fever was endemic demonstrated a dramatic increase in the density of rodents immediately preceding an outbreak of human disease (Mills et al., 1992). During an outbreak of Bolivian hemorrhagic fever in San Joaquin, nearly 3,000 rodents (C. callosus) (about 10 per household) were removed during a 3-week period, apparently contributing to the rapid decline in new cases (Mercado, 1975). Changes in resources and predators that affect the abundance of rodents, combined with patterns of agricultural production and land use, appear to be the major determinants of risk for many arenaviral diseases.
The emergence of Sin Nombre virus and other hantaviral agents provides a textbook example of the effect of ecological forces on rodent distribution and abundance (Nichol et al., 1993). In 1993, an outbreak of acute respiratory distress disease occurred in the southwestern United States, with the initial cases occurring predominantly among Native Americans. The case fatality rate was approximately 60 percent, causing widespread anxiety and enormous media interest in this newly emerged disease. Sin Nombre virus (genus Hantavirus, family Bunyaviridae) was identified as the etiologic agent of this disease, designated hantavirus pulmonary syndrome (Nichol et al., 1993; Elliott et al., 1994). This finding was unexpected; the only other hantaviruses known in the United States at that time were Prospect Hill virus, which was not known to cause human illness, and Seoul virus, which had been associated with mild renal illnesses in humans in the eastern portion of the country (Glass et al., 1994). Thus, no a priori reason existed to associate the acute respiratory disease outbreak in 1993 with hantavirus infection.
Hantaviruses are found worldwide and are major causes of morbidity and mortality in Asia and Europe (Schmaljohn and Hjelle, 1997). In Eurasia, Hantaan virus infections have been associated with illnesses causing signifi-